Consumption of salt or alcohol produces a hyperosmotic solution in the stomach due to the low molecular weights of these substances. Because the gastric mucosa is relatively impermeable to both polar solutes and to water, the gastric lumen tends to remain hyperosmotic and the gastric mucosa undergoes large reduction in the electrical potential difference and in the rate of acid secretion. One objective of these studies will be the clarification of the hyperosmotic alterations in the gastric mucosa. Reductions in potential difference and acid secretion after salt or ethanol treatment most probably involve inhibition of one or more of the active ion transport processes in this tissue. The in vitro flux chamber technique employing radioisotopes can unambiguously clarify this possible mechanism of hyperosmotic action in gastric mucosa. A second objective will be an investigation into the interrelationship between solute, especially potassium chloride, and ethanol in the stomach. In hyperosmotic, but not excessive concentrations, potassium chloride inhibits the absorption of ethanol from the stomach. The findings that this effect is not reproducible with equimolal concentrations of sodium chloride point to a specific role of the potassium ion in this process. These effects are presently unexplained since alcohol absorption is generally considered to be a diffusion process and should therefore be independent of any other ions or soluble substances in the gastric or intestinal fluid. The flux chamber method can be used to clarify these important findings. Finally, the actions of ethanol and concentrated solute must alter the basic biochemical pathways that mediate transport through the gastric mucosa. The pentose phosphate shunt is usually active in gastric mucosa and very likely can be altered in hyperosmotic media. The third objective will therefore be a determination of the relation between the pentose phosphate shunt and hyperosmotic actions.